Neurology Flashcards
What are the causes of Virtigo?
Benign paroxysmal positional vertigo. Acute labyrinthitis Meniere's Disease Ototoxicity Acoustic Neuroma Herpes Zoster Traumatic damage Stroke/TIA Migraine Alcohol intoxication
What is BPPV? It’s cause and symptoms?
Condition that causes sudden onset of dizziness associated with head movement.
Causes - usually idiopathic. If young = trauma.
Symptoms - Episodic (10-20 secs) virtigo associated with change of head position. Can be associated with nausea
What features are not associated with BPPV?
Tinnitus
Hearing Loss
Investigations for BPPV?
Family history of RA / back pain - may complicated further examinations
Ear examination
Dix-Hallpike test -
Management of BPPV?
Watch and wait - is this acceptable for the patient?
Epley manoeuvre
Consider Brandt-Daroff exercises. (vestibular rehabilitation)
Betahistine is commonly used (histamine analogue) but not very effective.
What is a Dix-Hallpike test and what is it used for?
Test for BPPV.
Patient sites up, turns head 45o in one direction. Lower patient in this position, make sure head is 30o below horizontal. Observe for rotatory nystagmus and vertigo.
Should be performed, tilting the head both left and right.
What is the Epley Manoeuvre and what is it used for?
Used for the management of BPPV.
With patient lying down, rotate head 90o. Ask patient to turn to that side whilst lying down. Turn head 90o so the head is facing the floor. Ask patient to sit up maintaining the direction of the head tilt. Realign head and flex neck downwards.
What is meniere’s disease and what are the symptoms?
Disorder of the inner ear. Characterised by pressure and dilatation of the endolymphatic system.
Symptoms - recurrent episodes of vertigo (>20 mins each), tinnitus and hearing loss (sensorineural). Vertigo is usually the prominent symptom
a sensation of aural fullness or pressure is now recognised as being common
nystagmus and a positive Romberg test
episodes last minutes to hours
typically symptoms are unilateral but bilateral symptoms may develop after a number of years
What is the classic triad of meniere’s disease?
Vertigo (recurrent)
Tinnitus
Fluctuating hear loss
Usually unilateral
Investigations for meniere’s disease?
ENT assessment to confirm diagnosis.
Refer to audiology
Admit if symptoms severe - IV labyrinthine sedatives (meclozine, promethazine) and fluids.
Second line - Diazepam or Prochlorperazine.
Betahistine for prevention.
Reassurance. Inform the DVLA.
What is acute labyrinthitis and what are its symptoms?
Also known as vestibular neuonitis.
Vertigo following a viral infection.
Features - Abrupt onset of severe vertigo (recurrent, lasting hours), nausea and vomiting.
Horizonal nystagmus is common.
NO DEAFNESS OR TINNITUS.
What is the treatment of acute labyrinthitis?
Vestibular rehabilitation exercises for those with chronic symptoms.
Buccal or IM prochlorperazine for those with acute severe symptoms.
Less severe = proclorperazine or anti-histamines.
What is acoustic neuroma and what are the symptoms?
Schwannoma from the vestibular nerve (rare tumour of the nervous system).
Growth rate = 1mm/year
Tumours slow growing and often benign
Symptoms - unilateral hearing loss with vertigo occurring later. Progressive = cranial nerves affected -V (absent corneal reflex), VI, IX, X) Raised ICP if advanced. Bilateral = NF2
Acoustic Neuroma treatment.
Refer urgently to ENT.
Surgery, radiotherapy or observation.
Acoustic Neuroma Investigation
ENT referral (Urgent) MRI of cerebellopontine angle is investigation of choice Audiometry is important. (
Syncope differentials
Reflex (vasovagal, situational, carotid sinus hypersensitivity, atypical) Orthostatic hypotension Cardiac syncope (arrhythmia, structural heart disease)
Common examinations for syncope.
Cardiac examination
ECG (including 24h)
Blood pressures (standing up and lying down)
Table tilt test
What is vasovagal syncope, signs, management?
Type of reflex syncope. Most common cause of fainting.
Caused by emotional distress (prolonged standing in heat). Common in young adults/adolescents.
Classic faint.
Benign - reassurance and trigger recognition. Avoid BP lowering agents.
Cardiac syncope. Causes, investigations, management.
Causes - arrhythmias, bradycardia. Can also be tachycardia.
Structural - Hypertrophy, valvular, MI
Others - pulmonary embolism.
Cardio examination ECG 24 hr ECG U&E's, FBC, Ca2+, glucose Echo CT/MRI brain ABG (pulmonary embolism, low CO2 suggests hyperventilation)
How do you classify epilepsy?
Either by seizure types of epilepsy syndrome.
Seizure types - Focal (starts in one place but can spread), generalised (both hemispheres affected).
Epilepsy syndrome - juvenille, Dravets
Focal seizure classifications.
Without impairment of consciousness or with.
Frontal movements - posturing (prolonged extension or flexion of the limbs) or peddling. Motor arrest subtle behavioural changes. Language can be affected as well.
Parietal - sensory disturbances such as tingling, numbness or pain
Can also have motor symptoms (if spread to the pre-central gyrus)
Temporal - automatisms (complex motor phenomena with unconsciousness - lip-smacking, chewing, swallowing)
Deja Vu
Emotional disturbance - tremor, panic anger
Hallucinations - smell, taste sound
Occipital - Visual disturbances (spots, lines, flashes)
General seizure classifications
Tonic-clonic - loss of consciousness, limbs stiffen (tonic), then jerk (clonic)
Absence seizure - begin in childhood, sharp onset and offset, eyelid twitching.
Myoclonic - shock-like contraction of the limbs, without impairment.
Atonic - sudden loss of muscle tone causing falls.
Diagnosis of Epilepsy
All patients with a seizure must be referred to specialist.
Take a thorough examination and establish the type of seizure.
Rule out provoking causes - trauma, stroke, haemorrhage, raised ICP, alcohol or benzodiazepine withdrawal
Metabolic causes - hypoxia, hypernatraemia, hypocalcaemia, hyperglycaemia.
Infection - meningitis
Drugs - cocaine, tryclyclics.
Investigations - Bloods (see for above). ECG. Consider EEG
MRI - structual cause
Drug levels - anti-eplieptic medication
DVLA
Headache differentials
Tension headache Glaucoma Migraine Trigeminal neuralgia Cluster headache Meningitis Sinusitis Head injury (extradural, subdural, subarachnoid)
Characteristics and management of a tension headache
“tight band across the forehead. Symptoms tend to be bilateral.
Lower intensity than a migraine. Also no aura, N+V
May be related to stress.
Other triggers: Dehydration, alcohol, skipping meals
Can coexist with a migraine.
NICE - Acute = aspirin, paracetamol or NSAID as first-line.
Prophylaxis - 10 sessions of acupuncture over 5-8 weeks
Low-dose amitryptyline
Above is for chronic tension-type (occuring 15 days or more per month)
Characteristic of a cluster headache (+risk factors)
Intense pain around the eye.
Usual presentation is a headache and a red, watery eye with nasal congestion/rhinorrhoea
Other symptoms - Lacrimation, eyelid oedema, facial/forehead sweating, miosis (constriction) and/or ptosis
Frequency - 1 every other day - 8 times a day
Clustered for 6-12 weeks followed by pain free periods
Most commonly affects men in their 20s or older who are smokers, family history, male sex and smoking/alcohol are risk factors.
Management of a cluster headache
C - reassurance, lifestyle changes - alcohol and smoking avoidance (triggers)
M - Acute Attacks - 100% oxygen (15 min via non-rebreather) - caution if COPD and subcut sumatriptan
Prophylaxis - Verapamil or prednisolone
S - Not much place but optical nerve stimulation may have a role in preventative medically-refractory chronic cluster headaches. (very last line management)
Differentials / investigations of a cluster headache
Migraine Paroxysmal hemicrania Trigeminal neuralgia Giant cell arteritis Headache associated with sexual activity Angle-closure glaucoma
Brain CT / MRI - rule out secondary causes (tumour, cavernous sinus pathology) (normal in cluster)
ESR - Exclude giant cell arteritis if over 50.
Pituitary function tests ?
Trigeminal Neuralgia Symptoms, investigations
Facial pain syndrome in the distribution of 1 or more divisions of the trigeminal nerve.
Symptoms - paroxysms of intense, stabbing pain lasting seconds in the trigeminal nerve area (V2 and V3). Face screws with pain.
Triggers - washing affected area, shaving, eating, talking
Typically male >50.
AGE AND MS are risk factors.
Investigations - clinical diagnosis THINK SECONDARY CAUSES = intra-oral X-ray (if dental cause suspected - dental caries, fracture). MRI - tumour, infarct, MS plaque
Trigeminal Neuralgia management
Medical preferred:
Anticonvulsants - Carbamazepine 1st line
2nd line - Topiramate
3rd line - gabapentin, lamotrigine
Consider baclofen (anti-spasmodic if resistant to the above)
For medically resistant - surgery = microvascular decompression (surgery to the compressive loop)
Migraine Presentation
Chronic, genetically determined, episodic neurological disorder that usually presents early-to-mid life.
Risk factors - family history, childhood motion sickness, caffeine, high altitude, female sex, menstruation, divorced, widowed or separated. Stress, overuse of headache medication, lack of sleep.
Prolonged headache - unilateral often. Throbbing/pulsing. Aura (blurred visiob) Hemiplegic disabling Lasts 4-72 hours Photophobia N+V Associated with triggers - worse with activity, caffeine, sex, chocolate, dehydration
Investigations for a migraine
Clinical diagnosis
ESR - rule out temporal arteritis (>50)
LP - abnormal if caused by subarach, meningitis,
MRI Brain (with contrast) - recommended for all concerning headaches. - may identify space occupying lesion or ischaemia
CT without contrast - emergency evaluation of acute headache (evaluate for intracranial haemorrhage)
Acute Migraine Management
Mild-moderate = NSAIDs / paracetamol + anti-emetic (metoclopramide), hydration
Severe = Triptan (almotriptan, sumatriptan). + same as above
IF PREGNANT = PARACETAMOL, ANTI-EMETIC, HYDRATION, MAGNESIUM
A+E severe = rescue therapy - metoclopramide or prochlorperazine + dipenhydramine or triptan + oxygen + IV corticosteroid
Ongoing Migraine Management
C - trigger avoidance and behavioural modification (relaxation/CBT), avoid caffeiene, cheese, chocolate etc.
M - NON-PREGNANT - cycle control (hormonal therapy if menstrual associated). Magnesium, triptan (frovatriptan or zolmitriptan) ?? or is it topiramate
Basically - propranolol, amitriptyline, or topiramate
verapamil (for hemiplegic migraine)
Red Flags for Headaches
New onset in > 50 years old Immunocomprimised History of malignancy known to metastasis to the brain Vomiting Impairment of consciousness Thunderclap Focal neurological symptoms Change in characteristic Abnormal neurological examination Headache with changes in posture Jaw claudication Neck stiffness Fever Personality change
Head Injury Approach
PROTECT AIRWAY AND C-SPINE Oxygen if sats <92% Stop blood loss Treat seizures with phenytoin Assess consciousness - intubate if GCS < 8 Neuro examination History Check for CSF leak from nose/ear
What are the indications for CT Head Immediately following a Head Injury (<1 HR)?
GCS < 13 on assessment GCS < 15 after 2 hours Suspected open or depressed skull fracture Sign of basal skull fracture Post-traumatic seizure Focal neurological deficit >1 episode of vomiting
What are the indications for CT Head within 8 hours following a Head Injury?
Age > 65
History of bleeding or clotting disorder
Dangerous mechanism of injury (pedestrian / cyclist hit by a car)
>30 mins of retrograde amnesia immediately before head injury.
Patient on warfarin.
Presentation of Extradural haemorrhage.
Typically trauma. Lucid interval.
Typically - initial loss of consciousness, briefly regains and then loses again.
Fixed, dilated pupil due to uncal herniation causing compression on third cranial nerve
Signs of raised ICP. Headache. Confusion, seizures, UMN signs. Dilated pupil (ispilateral)
What is an extradural haemorrhage and how are they sustained?
Collection of blood between the skull and dura.
Almost always caused by trauma (low-impact trauma).
Usually in the temporal area (pterion overlies the middle meningeal artery which is therefore vulnerable).
Investigations for Extradural haemorrhage
ABCDE Bedside obs Assess GCS Bloods - coag CT HEAD Biconvex/lens shaped, hyperdense collection around the surface of the brain, limited by suture lines of the skull
Management of extradural haemorrhage
ABCDE
Stablise - protect airway and C-spine
Transfer to neurosurgery for clot evacuation / ligation of bleeding airway
Mannitol to reduce ICP
What is a subdural haematoma, risk factors and how are they caused?
Collection of blood beneath the dural layer of the meninges.
Risk factors: 3A’s - Age, Alcohol and Anticoagulation (also coagulopathy)
Cause: High impact trauma, can therefore be associated with underlying brain injury.
Presentation of a subdural haematoma
Ranges from incidental finding to coma and coning (due to herniation)
Headache - gradually gets worse over hours-days
N+V
Diminished GCS
Losing consciousness
Seizures, sensory changes if getting worse
Signs of raised ICP
Investigations for a subdural haematoma
ABCDE
Basic obs / GCS
Non-contrast CT (standard choice in suspected haematoma). - will see a crescent shape collection of blood (not limited by suture lines). May also be midline shift
Consider MRI - assess extent of brain injury
Management of a subdural haematoma
ABCDE
Incubate if GCS < 8
Analgesia (pain can increase ICP)
Neurosurgical referral if persistent symptoms after initial assessment, focal neurological deficit or significant findings on CT.
If small haematoma (<10mm) and midline shift <10mm then observation, monitoring and follow up.
Prophylactic anti-emetics
Correction of coagulopathy
If large (>10 mm) or midline shift >5 mm then surgery - burr hole cranitomy.
Chronic - antiepileptics, elective surgery and coagulopathy correction.
Consider conservative - fall management, avoid activities that risk injury, controlled return to normal activities, having someone at home within first 24 hours to observe them.
What is stroke, the main types and the causes?
Stroke - rapid neurological deficit resulting from altered blood supply to the brain lasting > 24 hours
Types - Ischaemic, haemorrhagic (+TIA)
Ischaemic - 85% of strokes, emboli, typically arising from the heart (AF/MI/Valve disease), aortic arch, carotid artery (atheroma)
Haemorrhagic - intraparenchymal, subarachnoid. Cause - Vascular abnormality (aneurism), coagulopathy, vasculitis
Signs / symptoms of stroke
FAST Focal neurological signs - weak, numb Hemiplegia Sudden onset - often from waking up Symptoms worsen within hours Problems with speech Balance problems Also signs of source of emboli (ischaemic stroke) - murmur, fever (infective endocarditis, valve disease)
3 things to lookout for to help classify strokes?
Unilateral hemiparesis and/or hemisensory loss of face, arm or leg (UMN signs)
Visual signs - particularly homonymous hemianopia
Higher cognitive dysfunction - dysphagia, aphasia
Total Anterior Circulation Stroke (TACS) cause and presentation
Cause - occlusion of the internal carotid, cerebral or anterior cerebral arteries
Presentation - unilateral hemiparesis
Homonymous hemianopia
Higher cognitive dysfunction (dysphasia, aphasia)
Stroke investigations
Bloods - FBC, platelets, ESR, U+Es and LFTs, coag, glucose, cholesterol (know why we do these - notes)
CV tests - ECG, CXR, Echo, carotid duplex US
EMERGENCY NEUROIMAGING - CT (rules out haemorrhage and tumour but may be initially normal on an ischaemic stroke, also allows thrombolysis)
CT angiography (large vessel occlusion)
MRI - more sensitive than CT but less available
Stroke Management
ABCDE
Prevent hypoxia, hypoglycaemia, hypotension and infection
DVT prophylaxis if immobile
Admit to specialist stroke ward
MDT - physio, OT, speech and language therapy
Ischaemic - Thrombolysis if 4.5 hours of onset of symptoms and patient has not had previous haemorrhage or pregnant or uncontrolled HTN
Thrombectomy - if large vessel occlusion
Antiplatelets - Aspirin 300 mg OD for 24 hours post thrombolysis. Continue for 2 weeks before switching to long-term antiplatelet.
Haemorrhagic stroke - neurosurgical referral
Secondary Prevention - Antiplatelet (clopidogrel 1st line followed by Aspirin + modified-release dipyridamole 2nd line).
Anticoag instead for anti-platelet if AF
Statins for all
Screen and treat HTN
Carotid endarterectomy or stentin if > 50% carotid stenosis
Lifestyle changes
When can you give thrombolysis for a stroke?
Haemorrhagic stroke excluded.
Patient presents within 4.5 hours on symptom onset
No previous intracranial haemorrhage, uncontrolled HTN or pregnant
Also no CI to thrombolysis
Thrombolysis = Alteplase or Tenecteplase
Multiple Sclerosis Presentation
Optic Neuritis - ranges from reduced vision and colour blindness to complete vision loss. May see RAPD, disc swelling
Transverse myelitis
Other: - Dysaesthesia (feeling like water trickling or electric shock). Motor - spastic weakness, cerebellar symptoms, dysphagia, constipation, fatigue, cognitive impairment
As MS becomes progressive - gradual accumulation of disability
